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Neurodegenerative > Stroke > Flashcards

Stroke Flashcards

1
Q

Stroke facts

A

2nd leading cause of death worldwide
20-33% die within 1-3 months
Largest cause of adult disability in uk
25% of cases on people under 65

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2
Q

What is a stroke

A

Brain attack caused by the disturbance of blood supply to the brain
Rapidly developing clinical symptoms, focal or global, leading to loss of cerebral function that can only be attributed to vascular origin

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3
Q

Acute effect of stroke vs chronic brain disease

A

Rapid presence of symptoms vs build up over time

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4
Q

Obstacle to emergency treatment of stroke

A

Don’t know they are having a stroke
Long time between stroke and getting to the hospital
F - face
A - arms
S - speech
T - time

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5
Q

Ischemic stroke

A

Blood clot so blood flow stops so cells don’t get oxygen

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6
Q

Haemorrhagic stroke

A

Rupture of blood vessels

Intracerebral haemorrhage - blood spilled over brain, 10% of strokes

Subarachnoid haemorrhage - 5% of stroke

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7
Q

Transient ischemia attack (TIA)

A

Ischdmic events
Resolves with 24 hrs
No tissue death

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8
Q

Intracerebral haemorrhage

A

Blood goes into the premnchyal, invades brain tissue, invades neurones and glial cells, haemoglobin comes out (some neurones sub lethal exposure but have effect)
Extracellular haemoglobin induces cell death mainly via oxidation and inflammation

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9
Q

Subarachnoid haemorrhage

A

Venous sinus leak
Invades subarahnoid space and spreads around brain at high pressure
Blood released into subarachnoid space clots almost immediately and disappears via clot lysis which starts shortly after SAH
Highest incidence of death and disability and in younger people

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10
Q

Cerebral venous sinus thrombosis (CVST) EXTRA READING

A
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11
Q

Ischemic stroke

A

Aka thrombotic
85% of strokes
Usually in medial cerebral artery - arm and facial weakness, speech affected but depends on location Lenticulostriate arteries in lacunar stroke (most common, the small areas following MCA) - weakness on one side of the body

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12
Q

The brain needs to be adequately perfumed

A

Uses up most energy
Expensive to run in term of energy (ATP)
20% of energy
15% of cardiac output
(Sodium/potassium pump)

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13
Q

Brainstem stroke syndromes

A

Can affect fibre tracts (eg spinothalamic tract, nuclei (of cranial nerves) and physiological functions (eg consciousness and arousal)

Occlusion of vessel in posterior circulation

Stroke syndromes: medulla - wallenbergs syndrome, midbrain - webers syndrome, pons - locked in syndrome

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14
Q

Clinical features of brainstem strokes: tracts

A

Motor/sensory disturbance
Ataxia
Horners syndrome

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15
Q

Clinical features of brainstem strokes: nuclei

A

Cranial nerve dysfunction

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16
Q

Clinical features of brainstem strokes: physiological centres

A

Loss of consciousness

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17
Q

Stroke progression

A

Rapid - o2 depletion, energy failure, terminal depol, ion homeostasis failure (minutes)
Secondary - excitotoxicity, SD like depols, disturbance of ion homeostasis (hours to days)
Delayed - inflammation, apoptosis (days to weeks)

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18
Q

Current treatments for stroke

A

Antiplatelets
Clot busting agent aka alteplase
Anticoagulants
Carotid endarterectomy
Statins
Anti hypertensives
Neurosurgery- remove blood and repair burst blood vessels

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19
Q

Clot busting agent aka alteplase

A

Mainly used
Has to be given within 4 hrs so only 8% of patients eligible

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20
Q

Correct diagnosis extremely important

A

Eg Haemorrhagic cannot be given clot busting or will bleed to death
Must act fast for treatments

21
Q

How is the clinical outcome of stroke measured

A

National institutes of health stroke scale (NIHSS)
Bigger the score the worse off they are
Improved outcome with earlier treatment

22
Q

Risk factors of stroke

A

High blood pressure
Elevated cholesterol level
Smoking
Physical inactivity
Obesity
Alcohol consumption
60-80 % cumulative stroke risk

Non modifiable risk factors - older age, race (Hispanic, black), maternal history of stroke, sex (makes), diabetes

23
Q

How do risk factors increase the propensity to stroke

A

Structure and function of blood vessels - artherosclerosis, stiffening of arteries, narrowing thickening and tortuosity of aerterioles and capillaries eg atheroma, aneurysm

Interface with circulating blood - reduction/ alteration of cerebral flow (CBF)

Inflammatory cells - macrophages, T lymphocytes, mast cells, cascade - lesion development

24
Q

Stroke triggers can be identified in some patients

A

Neck trauma
Pregnancy/ postpartum
Systemic infection use of drugs
Mental stress

Exacerbation of vascular inflammation, activation of coagulation cascade leading to vascular occlusion and haemodynamic insufficiency

25
Q

Ten point plan for action

A

Awareness
Prevention
Patient involment
Act on warnings
Stroke as medical emergency
Stroke uni quality
Rehabilitation and community support
Participantion
Workforce
Service improvement

<50% of hospitals with acute stroke units have brain scanning available within 3 hrs

26
Q

Stroke (cells involved)

A

Interactions between glia, neurons, vascular cells, matrix components all relevant

27
Q

Normal aerobic metabolism

A

Oxygen + glucose lead to mitochondrial respiration to create cellular ATP produces and so ongoing consumption

28
Q

Stroke influence on aerobic respiration

A

Removal of mitochondrial respiration
So depletion of ATP
Accumulation of reactive oxygen species so even more ATP usage so intracellular acidification
Malfunction and cellular death

29
Q

Malfunction of ATP dependent processes

A

Enhanced consumption of cellular ATP
Profound loss of ioninc gradients so sustained rise in [glu]o (further loss of ionic gradients) and large elevations of intracellular calcium leading to excitotoxicity due to more ROS, proteases and mitochondrial Ca overload

30
Q

Inflammation

A

Ischemia evokes robust inflammatory response
Highly stereotyped and markers used to determine approximate age of cerebrovascular lesions
Stimulated glia and blood vessels communicate through complex signalling
Innate and adaptive immune systems used

31
Q

Early vascular, peri vascular and parenchyma events triggered by ischemia and reperfusion

A

Clot - stress/ pressure
Clot goes away - perfusion stress/pressure
Signals interact with BBB and may open it so may infiltrate the brain
Increase in ROE and decrease in nitric oxide produced by blood vessels
Interact with neurones and astrocytes

32
Q

Cell death and activation pattern, recognition receptors set the stage adaptive immunity

A

Neurones may release ATP or UTP in cells that have been opened by force and may leak out signal danger molecules
Eg HMGB1, HSP60, AB
Activate TLR 2 and 4

Lead to adaptive immunity, leukocyte infiltration, tissue damage and matrix degredation leading to DAMPs activation

Inflammation appliqués Ischemic lesion early on

33
Q

Resolution of inflammation and tissue repair

A

Microglia start to clear away dead cells
Start release neuro protective factors eg IL10 and TGF-B

Brain repair - neurones release helpful factors eg BDNF, VEGF to repair neurones and blood vessels

34
Q

Peripheral immunological changes after stroke

A

Blood, bone marrow, spleen and other lymphoid organs
White blood cell count and expression of cytokines and inflammatory markers up within hrs after ischemia then down within 1/2 days

Marked immuno depression - determinant of stroke morbidity and morality
Respiratory and UTIs

35
Q

Ischemia penumbra

A

Area of reduced perfusion sufficient to cause potentially reversible clinical deficits but insufficient to cause disrupted ionic homeostasis

36
Q

Contribution factors for irreversible damage of brain tissue in penumbra

A

Ischemic core
Irreversibly damaged tissue <20% baseline blood flow levels
Depleted ATP stores
Failure energy metabolism

Ischemic penumbra
Perinfract zone
Depressed tissue perfusion
Basal ATP lvls & o2 metabolism
Normal ion gradients
Electrical silence
Suppressed protein synthesis

Goes from salvageable tissue to dead within hrs and days

37
Q

MRI (DWI & PWI) - Acute ischemic stroke

A

Diffusion weighted imaging
Detects areas of restricted diffusion of water - bright in acute Ischemic stroke

Perfusion weighted imaging
Detects abnormal blood flow

Diffusion perfusion mismatch

38
Q

Salvageable brain to infractionsteps

A

Energy failure
Anoxic depol, excitotoxicity, oxidative stress, necrosis
Peri infract depol, calcium overload, mitochondrial damage
Inflammation, programmed cell death
Interacted tissue

39
Q

Studying stroke

A

Patients (post mortem, clinical trials)
Animal models (eg medial cerebral artery occlusion)
In vitro studies ( eg oxygen glucose deprivation)

40
Q

Possible stroke treatment - time sundowns and convo therapy approaches (EXTRA READING)

A
41
Q

Reversal of focal ischemia

A

Animal model (rat)
Mechanical occlusion of middle cerebral artery for 1 hr
Imaging of ATP and protein synthesis
Restoration of energy metabolism but not protein synthesis
Restoration of energy metabolism fails where protein synthesis did not recover

42
Q

Simulated ischemia in neurones causes sharp increase in glutamate receptor activation and anoxic depol (AD)

A

Glutamate mediate feedback mechanism that doesn’t let recover

Under Ischemic conditions, disruptions na+, k+ and pH gradients will cause transported to function in reverse leading to increased [extracellular glutamate]

43
Q

Potential therapy: glutamate/ca receptor blockers

A

Protect neurons from 1.5 hrs oxygen/glucose depreciation
Don’t protect >2 hrs

44
Q

Possible involvement of NMDARs, TRPM2 & 7 channels in anoxic neuronal death

A

Excessive activation of glutamate receptors
Activation of NMDA receptor subtype (voltage dependent)
Losing membrane potential, receptors bound to glutamate and open as cell is depolarised
Calcium influx
Activation of ion channels TRMP2 & 7
Interact with mitochondria so ROS
Essential interaction of nitric oxide synthase with PSD95 bound to NMDA receptors
Peroxinitrate (ROS) lead to cell death

45
Q

Nitric oxide

A

Multifunction biological messenger
Reduction in nitric oxide in vascular system - bad
High levels bad in neurones

Endothelial nitric oxide
Vasoregikatory effects
Antiaggregant
Antiprolifarative
Anti cell adhesion

Nitric oxide loss leads to vasoconstriction- platelet aggregation, leukocyte adhesion to endothelial cells, smooth muscle proliferation, key steps to vascular inflammation

46
Q

Inhibiting NOS reduces number of dead cells by NMDA application in cultured cells

A

[L-NAME] increase can rescue some cells as it is a NOD inhibitor

Knock down PSD-95 reduced number of dead neurons following NMDA application

Treatment with agent that perturbs PSD95 interactions - inefficient signalling through PSD 95 bound effector molecules by keeping NOS away

47
Q

Treatment of stroke with PSD95 inhibitor in primate brain

A

Decreased infraction compared to placebo condition
Primate - closer to humans

48
Q

N1-A treatment

A

40% decrease in morbidity
Functional independence - 10% increase
Good to give to all stroke types - give in ambulance, more likely to survive

Neurodegenerative (8 decks)

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